Superoxide dismutase in patients with chronic hepatitis C virus infection
Superoxide dismutase in patients with chronic hepatitis C virus infection
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DOI：
10.1016/s0891-5849(97)00437-1
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发表时间：
1998-05-01
影响因子：
7.4
通讯作者：
Prieto, J
中科院分区：
文献类型：
--
作者：
Larrea, E;Beloqui, O;Prieto, J
据报道，丙型肝炎病毒（HCV）可引起感染细胞的氧化应激。慢性丙型肝炎患者表现出肿瘤坏死因子α (TNF α)的增加，TNF α是一种通过刺激活性氧产生氧化应激的细胞因子；物种(ROS)。细胞对活性氧的防御包括锰超氧化物歧化酶（SOD）的过表达，这是一种诱导线粒体酶。为了研究HCV感染时细胞对氧化应激的防御作用，我们分析了慢性丙型肝炎患者肝脏和外周血单核细胞（PBMC）中Mn-SOD mRNA的表达，PBMC中Mn-SOD的表达在HCV感染患者中显著升高。治疗后有持续病毒学和生化反应的患者，其Mn-SOD明显低于病毒血症阳性患者。相比之下，慢性丙型肝炎患者的肝脏中Mn-SOD的表达没有增强。Mn-SOD mRNA的值与TNF α mRNA的表达、病毒载量或肝脏疾病的活动性无关。我们的研究结果表明，在HCV感染中，PBMC中存在Mn-SOD的诱导，但在肝脏中不存在，这表明该器官可能对氧化损伤的保护较弱。氧化应激可能参与HCV感染的发病机制。(C) 1998爱思唯尔科学有限公司
It has been reported that hepatitis C virus (HCV) may cause oxidative stress in infected cells. Patients with chronic hepatitis C exhibit an increased production of tumor necrosis factor-alpha (TNF alpha), a cytokine that can produce oxidative stress by stimulating the generation of reactive oxygen; species (ROS). Cell defense against ROS includes overexpression of Mn-superoxide dismutase (SOD), an inducible mitochondrial enzyme. To investigate cell defense against oxidative stress in HCV infection, we analyzed Mn-SOD mRNA in liver and in peripheral blood mononuclear cells (PBMC) from patients with chronic hepatitis C. Mn-SOD expression in PBMC was significantly increased in patients with HCV infection. Patients with sustained virological and biochemical response after therapy showed significantly lower Mn-SOD than patients with positive viremia. By contrast, Mn-SOD expression was not enhanced in the liver of patients with chronic hepatitis C. The values of Mn-SOD mRNA did not correlate with TNF alpha mRNA expression, viral load, or liver disease activity. Our results indicate that in HCV infection an induction of Mn-SOD was present in PBMC but absent in the liver, suggesting that this organ could be less protected against oxidative damage. Oxidative stress could participate in the pathogenesis of HCV infection. (C) 1998 Elsevier Science Inc.